Transcript APENDICITA ACUTA

CROHN’s DISEASE
Definition
 Granulomatous inflammatory disease, non specific, producing
necrosis and scaring of segments of gastrointestinal tract, which
is chronic and develops in recurring episodes :
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Acute phase (inflammation) = deep ulcers +/- perforations with abscess
formation and adhesions to adjacent structures
Chronic phase (fibrotic) = stricture formation.
Epidemiology
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High incidence in Scandinavia, N-V Europe and N-E of North America
Maximum incidence 20-30y;
More in Caucasians and Jewish population
More in women
CROHN’s DISEASE
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Ethiology:
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Unknown, probably multifactorial;
Potential factors involved:
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Genetic:
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Infectious:
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Sugested by the presence of granuloma
There is evidence for: viruses, bacteria and mycobacteria
Concomitent infections – E. coli, Clostridia, Campylobacter.
Alergies:
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Both twins develop disease;
Higher chance for an individual with familial clustering of Crohn’s;
Alergens in food and inhaled (fungus, molds) – anamnestic data, alergic testing
and more favorable results with specific hyposensitisation
Food:
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Elimination of weath flour and sugar = evident augmentation
CROHN’s DISEASE
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Immunological
Association with: arthritis, eritema nodosum: complex Ag-Ab
should be present
 Presence of Ab against different Ag structures and increase
concentration of IgA;
 Inflammatory infiltration and epitheliod granuloma formation =
high level immune cell mediated reaction against Ag structures;
 Corticoids and immune suppresive medication are highly effected
in Crohn’s disease;
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Probable: immune changes at the level of the mucosa with
hyperactive immune response against foreign Ag with cross
reaction and nonspecific tisular injury (innocent bystander)
CROHN’s DISEASE
CROHN’s DISEASE
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Pathology:
distribution:
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Terminal ileum and colon
90% of cases;
Oro pharinx, esophagus,
stomach and duodenum –
very rare;
Number of lesions
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Numerous lesions with
normal segments in between
ESSENTIAL of diagnostic
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Macroscopy
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Edema, eritema,
ulcerations, pseudopolyps,
fibrosis, sclerosis
Acute phase: bowel
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edema, enlarged, inflammed
(redish), inert
friabile;
Limits: very clearly delimited
Diseased areas are separated by
normal segments ;
Mesentery
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Edema, infiltrated with lymph
node hypertrophy
Sometimes more extensive then
bowel lesions
CROHN’s DISEASE
Presence of ulcer and
ulcerations – can be very
small or serpent like +
transverse ulcers producing
the image of islands
(cobblestone);
 Fissures and ulcers are the
origin of fistulas (enteroenteric, entero-colic, enterocutaneous, entero-vezical,
entero-vaginal)
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BOALA CROHN
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pseudopolyps
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Fibrosis, sclerosis, structure formation
Bowel wall very thick (up to 1cm)
Structures, short or long, unic or multiple;
Advanced stages: on long continuous stenosis
CROHN’s DISEASE
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Mycroscopy: characteristic = granuloma
with epithelioid giganto cellular cells :
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Giant cells + Langerhans cells + limphocytes (+ plasma
cells, eosinophils and PMN);
Never caseous necrosis≠tuberculosis;
Same inflammation in regional lymphnodes
Inflammatory infiltration is found through all
strata of the bowel wall;
CROHN’s DISEASE
Symptoms
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Insidios onset but mai also be sudden;
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A. symptoms associtaed with bowel problems
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PAIN
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DIARHEA
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Dull pain, medium intensity in the RLQ
Colicky when associated with obstruction: may be projected in the upper
abdomen.
4-6/day – watery or semisolid
Proportional to extent of lesions and activity of disease;
Bleeding per rectum: distal lesions.
NAUSEA, VOMITING, BORBORISM.
B. general symptoms
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fever 38 0C, +/- chills
Weight loss: diarhhea plus reduced surface for nutrient absorbtion
C. extraintestinal
Skin
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„metastatic” ulcers –
submamar, subpubian,
abdomen;
Parastomal ulceration
Anal and perianal
ulcerations:
eritema nodosum;
Aftoid oral ulcerations
Pyoderma gangrenosum.
CROHN’s DISEASE
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Joints
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Peripheral arthriits
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Spondilitis ankilopoetica
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Artralgia.
Hepatobiliary
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Sones due to interruption of
enterohepatic cycle;
Granulomatous hepatitis;
Steatosis ;
Cholangitis;
Fibrosis.
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Stones;
Hydronefrosis;
Fistula.
Ocular
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Urinary
Iridociclitis ;
keratitis;
conjunctivitis;
uveitis
Hematological
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anemia;
trombocitosis;
limfocitosis – B12, ferum,
folic. acid deficit
CROHN’s DISEASE
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Clinical examination
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general: malnurishes, pale,
cutaneous lesions;
abdomen:
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inspection
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palpation
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Pain in the RLQ
Guarding: perforative
complications;
Palpable bowel loop in RLQ,
deep, badly delimited, painful.
percution
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nothing
Regional distension (stenosis);
P.O. scars – important
postapendectomy
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dull
ascultation
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borborism, sometime.
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perineal region
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rectal
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Perianal fistula;
ulcerations;
fissure.
Often nothing;
Sometimes diffuse inflammation.
Fistula
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entero-cutaneous  visible;
entero-vezical
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disuria, polakiuria
pneumofecaluria.
recto-vaginal – symptoms and
visible on direct examination.
in the gallbladder: similar with
acute cholecistitis
retroperitoneal – diffuse celulitis
(very severe but very rare)
CROHN’s DISEASE
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Paraclinical
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Lab
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anemia – most oftem microcytic, hypochromc but
macrocytic anemia can develop (B12 deficit)
leucocitosis
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In acute phase
in complications (absces, fistula)
trombocitosis
ESR increased;
Electrolite embalance due to diarhea
Radiology - barium meal
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Alternation of normal and affected areas
Early stages
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nonspecific;
irregular folds, thickened folds;
Ulcers: deep in the wall aspect of rose thorn
associating 3 aspects
Pseudopolyps;
 Small spiculiform lateral ulcerations
 Large ulcers ;
IRREGULAR COBLESTONE
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Advanced stages
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No more folds;
Rigid stenotic tube
Stenosis + distended segments above;
Fistulas.
particular
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Terminal ileum – rigid cord;
Cecum – filling defect on the inner border +
retraction.
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Endoscopy GOLD STANDARD
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Small lesions + biopsy + extent of
lesions + monitor
Rectoscopia:
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75% normal;
Coblestones aspect
Ulcers or stenosis
friable mucosa that bleeds on touch.
Colonoscopy – similar + ileum!!!
Gastroscopy
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Biopsy
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Others:
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Deep + multiple
Even in normal area.
Plain abdominal X-ray – in
onclusive disease;
Bone X-ray for associated
bone disease;
Fistulography.
Laparoscopy
CROHN’s DISEASE
Diagnostic: positive
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Clinical scenario
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Radilogy
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segmentary, discontinuous lesions and asymetric lesion;
Deep transmural ulcers;
„cobblestone”, „string sign”, presence of pseudopolipilor;
Stenosis and fistula.
Endoscopy
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Young pt with diarhhea, abdominal pain I RLQ (often) +/- mass on
palpation +/- fissure or fistula perianal..
Skip lesions;
Multiple ulcers associated with edematous mucosa +/- stenosis
Pathology
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epithelio-giganto-celular granuloma;
lymphocytes and plasma cells infiltration - suggestive
BOALA CROHN
Diferential 1. Ileal disease
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Acute ileitis
Acute apendicitis, apendiceal plastic peritonitis.
tuberculosis
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Adnexal tumors.
Ileal carcinoid tumors: carcinoid syndrome
Radiation enteritis
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More general signs and PPD+;
Biopsy.
After RXT and diseapears after months.
Cecal tumors – local aspects may be
misleading
BOALA CROHN
Diferential 2. colonic disease
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Ulcerative colitis
Colonic cahnges in laxative abuse
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Watery diarrhea in a person that uses laxatives
Rx – loss of haustrations and signs of iritable bowel
syndrome.
Ischemic colitis
Diverticulosis
Cancer
Poliposis
IBS
Complications local
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Abscess formation
Fistula
Stenosis
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Inflamatory or scars;
Incomplete obstruction
GI Bleeding - mostly from colic
origin
Perforation: free perforation with
peritonitis is very unusual.
Toxic megacolon – rare but very
serious disease
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Toxic status + fever + major
abdominal pain + bloody and mucus
diarrhea + abdominal distension
RX massive distension and
destructuring
Complications - general
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Extraintestinal may be considered part of the disease or
complications if severe
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Cutaneous, joints, liver, small vessels (thromboembolic disease,
Takayashu disease
Renal
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Neuropsyhic:
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Sciesures or tetany due to hypoC and hypoMg
Anorexia
Psihosis.
Malabrobtion with consequences on growth.
Amiloidosis (visceral and renal) – after 10 years of evolution
Endocrine:
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Urinary lithiasis
Obstructions due to mechanical compression of urethers;
amenoreea, infertility, late puberty
Small bowel or colonic cancer – after many years
TREATMENT
Medical
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General
Bed rest
Psihoterapy;
Dietary
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hypercaloric, hperproteic,
vitamines (folic, A, D, K, C,
B12) and minerals (Ca++,
Mg++, K+, Fe++, Zn++);
EXCLUDE:
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Food with many fibers
)mostly in pt with stenosis;
Milk – intolerance ;
Lipids in case of
malabsorbtion of lipids.
MAJOR situations- TPN
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Symptomatic
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Pain therapy
Treat diarrhea:
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codeine phosphat
Treat dep on cause:
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No spices ;
No milk - intolerance;
Bile salts: interruption of the
liver-enteric cycle;
Atb - infection
Treat electrolytic imbalance.
Traet anemia : Fe, B12, folic
acid
TREATMENT - pathogenic
ANTIINFLAMMATORY
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5ASA
Salazopirine: better in colonic disease
ANTIBIOTICS
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CORTICOIDS - may induce remission
IMMUNE SUPRESSION
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Metronidazol.;
Chinolone
Azatioprina (Imuran) – prevention of recurrence;
6 mercaptopurine
Cyclosporine
Methotrexat
BIOLOGICAL Infliximab (Remicade)
TREATMENT
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SURGICAL
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Indications
Acute complications
 local complications – stenosis, fistula;
 Unclear diagnostic.
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Limited resection of involved bowel
Enterostomy – end later resection
TREATMENT
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A. Crohn ileocolic
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Indications:
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fistula;
obstruction;;
Percutaneous drainage and resections
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B. Colonic Crohn
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Indication
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TREATMENT
same;
megacolon toxic.
3 operaţii:
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proctocolectomy (abdomino-perineal) with permanent ileostomy;
Total colectomy and ileostomy but rectum in place;
Total colectomy plus ileorectal anastomosis.
TREATMENT
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Anal and perianal
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Treatment of the abscess and fistula + treatment of Crohns.
If refractory disease n the rectum - proctectomy
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Obstruction
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ileon:
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TREATMENT
Ileon resection;
Ileo-cecal resection
By pass.
colon:
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by-pass;
Ileostomy or colostomy.
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Stenosis
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TREATMENT
rezections
Stricture-plasty
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Cancer
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Long term complication
High risk for pt with long term Crohns, strictures and
scleroiss cholangitis
Colonoscopic monitoring – 2-3 y
Displastic lesions: colectomy
ULCERATIVE COLITIS
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Ethiology
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unknown
More frequent USA,
England, northern
countries;
Onset 18-30y
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Under 18 very severe;
Over 50 very unusual.
More often in male pt
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Genetic factors
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Numerous germs isolated but not clear;
Atb not very good;
Probably secondary and cause of recurrence .
Enzimatic
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Family clustering;
Possible implication of a defect in IgA production
Infection
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UC
Increased synthesis of lizozim – destroys the protective mucus;
Not clear if primary or secundary .
Psihosomatic
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Patients are more psichologically vulnerable to conflict;
Emotional problems involved in onset and maintenance of new
episodes
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Pathology
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Macroscopy
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serosa
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Reddish and glittering;
Pale or pale with red spots.
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Shortening of the length;
Narrow lumen;
No haustrations;
Thick wall (due to the muscle layer);
Friable, paper-like.
mesocolon
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normal.
advanced
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retracted;
Large lymph nodes.
Sometimes psudopolyps
Patches of renewed musosa
near the lesions
Intense renewal – mucosal
bridges and vegetations
chronic
initially
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red
Small erosions – ulcers
(superficial. Not deep);
brittle;
Continuous lesions
Wieschelmann pseudiopolyps
subacute:
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Very dilated bowel.
Severe
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Fulminant disease
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Distended, thin;
Advanced
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Initially:
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Acute:
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Intestinal wall
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chronic
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mucosa:
Acute
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Wide spread lesions with
incomplete healing of the
mucosa;
Thin mucosa;
UC
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UC
Particular aspects – affects only the mucosa of the rectum and the
colon
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First rectum then colon
The lower the segment the more aggressive the disease;
The lesions are continuous;
UC
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Microscopy:
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Dilation of vessels folllowed by haemmorhage;
limfocites and plasmocites;
Deep glands are full of neutrophils – abcess of the crypts –
ulcerations and pseudopolips.
histology:
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Granulocyte infiltration is specific
If inflammation spreads to all layers – toxic megacolon.
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UC
Clinic
digestive symptoms
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diarrhea:
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First in 30-50% cases;
Main symptom 4/5;
Feces in a sero-hematic liquid full of puss
2-3 up to 15-20 stools/day;
Sometimes just blood per anum
Abd pain:
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Colicky – left side
characteristic:
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tenesmus;
No more pain after a stool is passed.
General
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Fever –septic;
Weight loss;
Vomiting;
Tachycardia - depending on amount of lost fluids.
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Clinical exam
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abdomen:
 inspection:
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reduction of subcutaneous
tissue;
bloating - especially
supraumbilical - installation
may highlight acute toxic
dilatation of the colon.
percution:
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UC
timpanism increased in the
case of toxic dilatation of the
colon;
painful;
auscultation:
multiple air-liquid noises
uncomplicated ulcerative colitis
tranquility in ulcerative colitis
complicated by megacolon.
Rectal exam
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sphincter tone:
increased due to pain;
decreased in severe forms;
rectal wall:
rigid;
granular mucosa;
stricture areas;
Mucosa: endoscopy
inflammatory exudate in the
rectal mucosa, or the presence of
blood, mucus, pus;
highlights other injuries:
cancer, hemorrhoids, abscesses,
fistulas, etc..
UC
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stool:
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in severe forms, extensive:
stools are unformed, with feces
floating in a serous fluid, blood
mixed with mucus and pus;
bulky stools with much blood.
in mild forms
stool can be formed with
blood and mucus;
in forms limited to the rectum:
stools, wrapped in blood and
mucus;
emissions of blood and mucus
without stool.
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general:
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apathy or restlessness,
anxiety;
palor;
dehydration, malnutrition;
detection of systemic
events:
eye;
articulation;
skin.
UC
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Laboratory:
leukocytosis - active phases;
 anemia;
 hypoalbuminemia;
 electrolytes:
significant changes only in severe forms;
lowering of Na +, K +, Cl-, Mg + +;
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Radiology
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Simple x-ray or
radioscopy
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Always first
(perforation,
incontinence)
Active phase:
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No haustrations;
Thick wall;
Cobblestone aspect
– psudopolyps;
Distended lumen;
UC
UC
Late, advanced stages
 mucosal relief is deleted;
 haustations disappear
completely;
 size is reduced;
 linear shape;
 distensibility is greatly
reduced;
 angles rounded;
 sometimes stenosis;
 rigid tube (microcolia).
Endoscopy
Inititial stages:
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UC
Red mucosa with vessels visible;
Friable mucosa;
Bleeding is spontaneous and difuse;
Grainy aspect;
Blood, mucus and pus in the lumen;
Florid stages:
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Ulcerations that may converge with
one-another;
Crypt abscesses;
False membranes.
Late stages:
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Atrophy of the mucosa;
Lack of haustrations;
Pseudopolyps;
biopsy:
Exfoliative cytology
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CT, MRI
UC
UC
Local complications
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May appear in acute UC
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Perforation
Acute dilation
Massive bleeding (more
than 3000 ml in 24 hours
Perianal lessions
Due to chronic disease
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Stenosis of the rectum
and colon
Pseudopoliposis
Cancer
UC general complications
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articular
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most frequently;
5 categories:
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Rheumatoid arthritis;
Spondilitis;
Erythema nodosum;
Joint pain;
Acute toxic arteritis
Spondilitis is the only one that
can persist after surgery and
medical treatment.
ophtalmologic
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conjunctivitis; uveitis; iritis;
episcleritis; keratitis; retinitis.
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cutaneous and mucous:
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cutaneous
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Erythema nodosum;
pyoderma gangrenosum;
Urticaria, acnea, dermatitis.
mucous – stomatitis;
liver – chronic liver disease
and cirrhosis;
Kidney - stones,
hidronefrosis
UC
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Diferential
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Crohn’s disease
Colorectal cancer
Diseneteria
Ischemic colitis
Polyposis
Bacilarry colitis
Irritable bowel syndrome
Diverticulosis
Piles
UC
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Treatment
Objectives:
Reduce the time that the patient spends in acute stages of
the disease.
 Prevent relapses and complications;
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A. Treatment of the acute stage
1. bed rest
 2. food intake
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3-5 days of a colon sparing diet
 Small, frequent meals;
 No milk
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3. psihotherapy
 4. correct nutritional and hydroelectrolitical imbalances.
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5. antiinflammatories and
antibiotics
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a) salazopirin
b) 5-aminosalicilic acid
c) corticoids and ACTH
d) antibiotics
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fever;
sepsis.
e) immunosuppressive
treatment
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6-mercaptopurin;
6-tioguanin;
Azatioprin
Metrotrexate
Ciclosporin
UC
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B. Prevent relapse
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1. Salazopirin
1,5-2 g/day 6-9 months;
 2-2,5 g/day 10 days/month.
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2. diet.
 3. avoid psychological stress, respiratory or digestive
tract infections;
 4. follow up.
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C. Surgery
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1. total proctocolectomy
and permanent ileostomy
2. total colectomy, treatment
of the rectal stump and
reestablishment of the
continuity of the digestive
tract 6-12 months later
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Risc of a disease
progression or relapse
Cancer risk.
3. total colectomy with
ileorectal anastomosis in the
same procedure;
Diverticular disease
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Definition
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Herniation of the colic mucosa
through defects of the muscle layers
Frequency
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Incresed with aging:
Sex: ♂:♀ = 2:1;
Incidence:
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

Maximal in Western Europe
Minimal în Africa and Asia.
More frequent in urban patients
and in patients with stressfull jobs.
Diverticular disease

Aethiology

Precise cause is unknown.
Development of diverticulae:
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
Muscle contraction:
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

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Hipertrophy of the circular
musculature
Shortening of longitudinal fibers;
The result is pressure pockets that
push the mucosa throus the muscle
fibers
Weak spots in the colonic wall
Diverticular disease



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Weakening of the wall due to fatty inflammation;
Low fiber intake - constipation;
Psychological stress;
In time:


Stasis of feces – fecaliths – ulcerations of the mucosa due to
mechanical irritation – increase in septic fenomenae.
Closed cavity – increase in virulence of germs and increase in mucus
secretion – congestion – inflammation – thickening of the wall
Pathology


Number – rarely unique:
Topography:

Entire colon:



Structure:



Most frequent on descending
and sigmoid;
Rectum is not affected.
Body and sometimes also a
neck
!False diverticulae!
Colon:



Shortened and thickened
teniae;
Arches of circular
musculature between
diverticulae;
Normal nercous plexuses.

Diagnosis

Clinical:
Asimptomatic
Atypical digestive
symptoms:
Symptoms usually due to
complications.
Paraclinical:
Barium enema, colonoscopy






Complications

A. Diverticulitis
 30% of patients with diverticular disease ;




simptoms:






One or more diverticulae
Due to stasis of feces
peridiverticulitis
Very painful – left iliac fosa;
Irregular bowel habits;
Bloating;
Nausea;
Fever;
Clinical exam:




Tumor mass in left iliac fosa
painful;
Lower limit of tumor can be assessed on rectal digital exam
Above the tumor the descending colon is short and rigid

CT, US
Diverticular disease
B. Haemmorhage




Frequent due to vecinity of vessels ;
More frequent in the right colon;
clinical:




Large haemmorhage;
Rarely melena;
Reocurring frequently.
paraclinical:




scintigraphy
arteriography:
pancolonoscopy
laparotomy.
C. Fistulae - due to an

abscess:

exterior:


interiore:

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

colo-cutaneous
colo-enteric, colo-colic
colo-uretheral
colo-vesical
colo-uterine:
colo-vaginal
3 syndroms:



General septic;
Pericolic abscess;
Peritonitis

D. Perforation


First a pericolic abscess and then peritonitis
E. Obstruction


Mechanical - due to inflammation
clinical:



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Suboclusive syndrom
Low obstruction + fever:
Tumor mass in the left iliac fossa
Barium enema;
Colonoscopy + biopsy.

Medical
TREATMENT
 Profilaxis
of complications:
 Avoid
constipation;
 No spices;
 Mild antispastics;
 diverticulitis
 High
fiber intake and laxatives;
 Antiinflammatory drugs
 Antibiotics.
Surgery


Segmental resection
of affected colon;
In emergency – 2
step procedure:


Hartmann I
followed by
reestablishment of
continuity
Colostomy in
emergency followed
by resection with
anastomosis after
acute fase passes.